Calcium action potentials restricted to distal apical dendrites of rat neocortical pyramidal neurons.
1. Simultaneous whole-cell voltage and Ca2+ fluorescence measurements were made from the distal apical dendrites and the soma of thick tufted pyramidal neurons in layer 5 of 4-week-old (P28-32) rat neocortex slices to investigate whether activation of distal synaptic inputs can initiate regenerative responses in dendrites. 2. Dual whole-cell voltage recordings from the distal apical trunk and primary tuft branches (540-940 microns distal to the soma) showed that distal synaptic stimulation (upper layer 2) evoking a subthreshold depolarization at the soma could initiate regenerative potentials in distal branches of the apical tuft which were either graded or all-or-none. These regenerative potentials did not propagate actively to the soma and axon. 3. Calcium fluorescence measurements along the apical dendrites indicated that the regenerative potentials were associated with a transient increase in the concentration of intracellular free calcium ([Ca2+]i) restricted to distal dendrites. 4. Cadmium added to the bath solution blocked both the all-or-more dendritic regenerative potentials and local dendritic [Ca2+]i transients evoked by distal dendritic current injection. Thus, the regenerative potentials in distal dendrites represent local Ca2+ action potentials. 5. Initiation of distal Ca2+ action potentials by a synaptic stimulus required coactivation of AMPA- and NMDA-type glutamate receptor channels. 6. It is concluded that in neocortical layer 5 pyramidal neurons of P28-32 animals glutamatergic synaptic inputs to the distal apical dendrites can be amplified via local Ca2+ action potentials which do not reach threshold for axonal AP initiation. As amplification of distal excitatory synaptic input is associated with a localized increase in [Ca2+]i these Ca2+ action potentials could control the synaptic efficacy of the distal cortico-cortical inputs to layer 5 pyramidal neurons.
Schiller
J
J
Abteilung Zellphysiologie, Max-Planck-Institut für medizinische Forschung, Heidelberg, Germany.
Schiller
Y
Y
Stuart
G
G
Sakmann
B
B
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001369:Axons / Q000502:physiology; D002118:Calcium / Q000502:physiology*; D003712:Dendrites / Q000502:physiology*; D004553:Electric Conductivity; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D005453:Fluorescence; D066298:In Vitro Techniques; D007555:Isoxazoles / Q000494:pharmacology; D019579:Neocortex / Q000502:physiology* / Q000648:ultrastructure; D018408:Patch-Clamp Techniques; D011422:Propionates / Q000494:pharmacology; D017966:Pyramidal Cells / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology
D018690:Excitatory Amino Acid Agonists; D007555:Isoxazoles; D011422:Propionates; D016194:Receptors, N-Methyl-D-Aspartate; C081662:alpha-amino-3-hydroxy-5-tert-butyl-4-isoxazolepropionate; D002118:Calcium